By James O. Armitage, Karen H. Antman

ISBN-10: 0683306545

ISBN-13: 9780683306545

Univ. of Nebraska, Omaha. Reference at the easy and scientific technological know-how of dose-intensive melanoma treatment. For hematologists, oncologists, and fellows within the box. past version: c1995. Halftone illustrations with a couple of colour plates. vast references. DNLM: Neoplasms--drug treatment. additional to Brandon-Hill scientific checklist in April 2001.

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Additional info for High-Dose Cancer Therapy: Pharmacology, Hematopoietins, Stem Cells, 3rd edition

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The effect on tumor cell killing of adding pentoxifylline to cyclophosphamide was similar to that seen with thiotepa (110) (see Fig. 11). Cyclophosphamide killed increasing numbers of FSaIIC tumor cells with increasing dose of the drug in a log-linear manner. A single dose of pentoxifylline (100 mg/kg) immediately before treatment with cyclophosphamide increased tumor cell killing about twofold. 31 over 24 hours with cyclophosphamide given immediately after the third injection of pentoxifylline produced a threefold increase in tumor cell killing with 100 mg/kg of cyclophosphamide, increasing to ninefold with 500 mg/kg of cyclophosphamide.

7. During the MRD phase, the ratios of the extremes ranged from a factor of 36 to greater than 13,000 from one rat to another. The variability among bones of comparable size was estimated by studying the ribs from each individual animal. 4 to greater than 320 after chemotherapy. 19 bones cut into slices. 3 and in MRD from 4 to 28,000. These data may partly explain the sometimes conflicting observations in leukemic patients. In the BNML model, high doses of drugs are necessary to completely eliminate MRD even when the tumor load is as small as 1 Ã 104 cells (25).

Points are means; bars are standard error of the mean. Effects of Repetitive Cycles of Alkylating Agents Allowing an interval between drug treatments produces a biologically complex situation involving lysis and removal of dead cells, as well as stasis or proliferation of surviving cells. Survival may be due to preexisting biochemical factors conferring resistance or to induction of biochemical changes conferring resistance. The current best solution may be to administer the most effective agents early and to develop treatment sequences in which overlapping mechanisms of resistance do not occur.

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High-Dose Cancer Therapy: Pharmacology, Hematopoietins, Stem Cells, 3rd edition by James O. Armitage, Karen H. Antman

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